The search for genetically influenced markers of a predisposition toward alcohol abuse is based on an extensive literature supporting the importance of probable genetic factors in alcoholism. Since humans most likely consume alcohol for its pharmacological effects, it is reasonable to assume that the ingestion of alcohol results in neural effects that are characterized by genetic differences. There is currently much evidence to suggest that neurophysiological effects of alcohol in animals and in humans are strongly determined by genetic factors. The study of the neuropharmacogenetic effects of acute alcohol intake in individuals with a positive family history of alcohol abuse compared to matched individuals with a negative family history is likely to provide valuable information concerning the potential vulnerability factors in alcoholism. We propose to extend our neurophysiological observations obtained in young boys (7-13 years) at high risk (HR) and low risk (LR) for alcoholism to a young male (19-25 years) high risk population (with a positive family history of alcohol abuse) and a matched low risk group (negative family history of alcohol abuse). We plan to use various evoked potential (EP) techniques to compare high risk and low risk males before and after the administration of placebo, 0.75 ml/kg and 1.1 ml/kg of alcohol. Neurophysiological studies will take place before the ingestion of any liquid and at 30, 60, and 120 minutes after drinking. We propose to use a number of EP techniques which are known to be sensitive to the effects of alcohol. Such as the brainstem auditory evoked response (BAER). We will study various components (N1, Nd, N2 and P3) of the auditory and visual event-related potentials (ERP). We propose to assess the recovery function (RF) of the N1 and P2 components of the ERP. Breathalyzer values and self-rating scales of alcohol effects will be collected at the same time as neurophysiological data. Finally the data obtained from the detailed family histories will be used to mathematically derive a quantitative index of risk for alcoholism. These data will be examined in relation to the EP data on the neuropharmacogenetic effects of alcohol. The identification of early markers of predisposition toward alcoholism in high risk individuals is important in elucidating etiological factors and in the rational development of prevention initiatives.